Sheridan R E
Neurotoxicology Branch, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010, USA.
Toxicon. 1996 Aug;34(8):849-55. doi: 10.1016/0041-0101(96)00040-2.
Botulinum neurotoxins (BoNT) are thought to enter cells through endocytotic vesicles where acidification is required for release of these toxins into the cytoplasm. Two ionophores, nigericin and monensin, that increase membrane permeability to H+ and K+ or H+, Na+ and K+, respectively, block vesicle acidification by acting as H+ shunts to neutralize pH gradients. Nanomolar concentrations of nigericin or monensin delayed development of blockade in BoNT-A or BoNT-B treated muscles two-to threefold over onset times in unprotected muscles. However, higher concentrations of the ionophores directly blocked synapses. Thus, nigericin and monensin could delay onset of BoNT paralysis only over a narrow range of concentrations.
肉毒杆菌神经毒素（BoNT）被认为通过内吞小泡进入细胞，这些毒素释放到细胞质中需要酸化环境。两种离子载体，尼日利亚菌素和莫能菌素，分别增加膜对H⁺和K⁺ 或H⁺、Na⁺和K⁺ 的通透性，通过作为H⁺ 分流器来中和pH梯度，从而阻断小泡酸化。纳摩尔浓度的尼日利亚菌素或莫能菌素使BoNT-A或BoNT-B处理的肌肉中阻滞的发展延迟，比未受保护的肌肉中的发作时间长两到三倍。然而，更高浓度的离子载体直接阻断突触。因此，尼日利亚菌素和莫能菌素仅在狭窄的浓度范围内能延迟BoNT麻痹的发作。
